Crops are biological monocultures under severe disease pressure from pathogenic bacteria, fungi and viruses. Cereal crops are the primary source of food for humans and their animals. The yield loss due to cereal plant diseases varies by crop, season and locale, but is estimated to exceed $100 billion worldwide (Brears and Ryals (1994) Agro-Food-Industry Hi-Tech July/August 10-13). Two major approaches to solve the problem are pesticide applications and the use of resistant germplasm. The source of this resistant is often wild species related to the crop plant (exotics), and such genes are introduced into new crop cultivars by laborious and time-consuming genetic backcrossing, to retain the favorable characteristics of the crop parent.
Effective genetic disease resistance in plants is governed by resistance (R) genes. Historically, introgressed exotic germplasm conferring disease resistance has been found to contain novel plant R genes. Plant R genes confer resistance to pathogen races bearing a cognate avirulence (avr) gene. The absence of either member of a cognate R/avr gene pair can result in disease. There are multiple R/avr cognate gene pairs in the plant and the pathogen, respectively, varying in the strength of the defense response they elicit.
The RAR1 gene of barley functions in disease resistance mediated by a subset of R genes (Peterhansel et al. (1997) Plant Cell 9:1397-1409). RAR1 has been cloned and encodes a protein with two novel Zn-binding (named CHORD) domains (Shirasu et al. (1999) Cell 99:355-366). This group also reported highly conserved RAR1 homologs in humans, Caenorhabitis elegans, Drosophila melanogaster, as well as in the model dicot Arabidopsis thaliana. 
Given the high degree of genomic synteny between cereals (Devos and Gale (2000) Plant Cell 12: 637-646), we reasoned that a full-length rice RAR1 gene should both exist and function in disease resistance in that species. Using our proprietary rice genomic database, a single rice RAR1 cDNA was cloned. The gene functions in mediating resistance by a subset of R genes in response to certain pathogen races. Over-expression of RAR1 confers enhanced disease resistance by mechanisms which are currently unclear.